Endocrine Abstracts

Background: Menopause is associated to body composition transformations, such as an increase in total fat mass (obesity), central fat mass and a decrease in lean body mass (sarcopenia). Body fat distribution also changes with age, with an increase in visceral abdominal fat and a decrease in subcutaneous abdominal fat. Moreover, an increase in visceral fat may lead to increase the secretion of pro-inflammatory adipokines that further promote insulin resistance as well as potentially having a direct catabolic effect on muscle. Thus, a vicious circle between muscle loss and fat gain may lead to more sarcopenia and then to further fat gain and inflammation (c-reactive protein (CRP)). Sarcopenic-obesity, which occurs in around 10% of postmenopausal women, has been reported to be a much pejorative condition of the development of physical disabilities, morbidity and mortality than either sarcopenia or obesity alone. In fact, being obese non-metabolically healthy with an inadequate muscle mass may represent the worse aspects of each condition. However, our group showed that obese women have higher cardiovascular risks than metabolically healthy sarcopenic-obese post-menopausal women.

Objective: The aim of this study is to examine if the degree of sarcopenia could influence the metabolic profile of sarcopenic-obese post-menopausal women.

Methods: Fifty-six postmenopausal sarcopenic-obese women were divided in 2 groups: class II sarcopenic (n=28), class I sarcopenic (n=27). Obesity was defined as total fat mass >35%. Appendicular muscle mass index (AMMI=(legs+arms FFM (kg))/height (m²)) was used to determined sarcopenia. Class I sarcopenia is considered as an AMMI <7.12 kg/m² and class II as < 6.29 kg/m². Lipid, glucose and inflammatory profiles were measured as energy metabolism and dietary intake. ANOVA was used to compare the groups (SPSS 17.00; P<0.05).

Results: No difference between groups for age, BMI, waist circumference, lipid profile or glucose profile was found. We observed significant differences between groups for fat-free mass (total and appendicular; P=0.001), viscera fat mass (P=0.045), resting energy expenditure (P=0.002), CRP (P=0.034) and total protein intake (g/d; P=0.011) animal protein intake (g/d/BW); P=0.037). Type II sarcopenia presented a lower amount of visceral fat for the same amount of abdominal fat, a lower resting energy expenditure, and a lower CRP. But surprisingly they consumed a higher amount a total and animal protein intake.

Discussion: Interestingly, this study showed that the metabolic profile is different regarding to the type of sarcopenia. In fact, type II sarcopenia seems to be more protective against cardiovascular risks than type I sarcopenia. Further studies are needed to confirm our results and explore if the index and the cut-point used to determine sarcopenia could explained the discrepancies in the literature. In fact, compared to osteoporosis or obesity diagnosis, no international consensus (definition and cut-point) are available for the sarcopenia.